American Association for Cancer Research

AACR Press Releases

AACR Debuts Frontiers in Basic Cancer Research Meeting

October 9, 2009

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PHILADELPHIA - The American Association for Cancer Research will host its first Frontiers in Basic Cancer Research Meeting in Boston from Oct. 8-11, 2009. The meeting is expected to draw nearly 500 leading scientists to present on high-profile topics like epigenetics, metastasis and systems biology, and create synergies among the many subfields of basic science.

Tyler Jacks, Ph.D., director of the David H. Koch Institute for Integrative Cancer Research at MIT and president of the AACR, hosted a news briefing to highlight some of the important research that will be presented at this meeting.

The press briefing took place on Oct. 9, 2009, at 12:30 p.m. ET, in the Stuart Room of the Boston Park Plaza Hotel

Download* the mp3 of the press briefing (5.17 MB, 22 minutes and 35 seconds)

"Basic science is the foundation of clinical research that leads to patient breakthroughs. These research projects are examples of work that is being done in the laboratory that will one day directly impact patient care," said Jacks.

Jacks cited Gleevec, the anti-leukemia drug that has revolutionized the prognosis of patients with leukemia, as an example of a patient breakthrough that began in the lab.

"What people often forget is that the laboratory work on Gleevec began 40 years before any patient was even treated. Progress is deliberate, but it does continue," said Jacks.

The following abstracts were presented at the press conference:

#A22. Pooled analysis of phosphatidylinositol 3-kinase (PI3K) pathway variants and risk of prostate cancer

Scientists have observed an association between a collection of PI3K gene variations and prostate cancer risk that became stronger after considering the patient's age at diagnosis and family history, according to data presented at the American Association for Cancer Research Frontiers in Basic Cancer Research Meeting.

Stella Koutros, Ph.D., a post-doctoral fellow at the National Cancer Institute, said this was the first time PI3K genes had been evaluated in this setting, though further studies are needed to confirm the relationship and determine the role of the pathway in prostate cancer etiology.

"We observed an association in a very large nested case-control study drawn from several prospective cohorts, but the information will need to be confirmed," said Koutros.

Koutros and colleagues observed 8,309 cases of prostate cancer and 9,286 controls. They examined 89 single nucleotide polymorphisms (SNP) on the following PI3K pathway genes: PIK3C2B, PIK3AP1, PIK3C2A, PIK3CD and PIK3R3.

They found that the SNP rs7556371 in PIK3C2B was significantly associated with between an 8 percent and 21 percent increased risk of prostate cancer overall.

Men who carried the rs7556371 risk allele had a 47 percent increased risk of early-onset prostate cancer (diagnosed at age 65 or younger) compared to men who did not carry the variant. Among men with a family history of the disease, those carrying the risk allele had a 57 percent increased risk of prostate cancer compared to men who did not carry the PI3K variation.

The greatest increase in risk was observed in men who had both a family history of prostate cancer and early-onset disease. Carriers of this risk allele had a 2.31-fold increased risk for prostate cancer compared to those without the PI3K variation. The variation was not associated with differences in disease aggressiveness.

#C49. AKT inhibitor has potent antitumor activity in human lung cancer xenograft models

Scientists at Cellceutix Corporation may have developed a new compound that could significantly delay lung tumor growth, according to data presented at the AACR Frontiers in Basic Cancer Research Meeting.

Lung cancer accounts for 215,000 new cases and 130,000 deaths in the United States every year, making it the single leading cause of cancer death. Non-small cell lung cancer accounts for 80 percent of all bronchogenic neoplasms, with 90 percent of diagnosed patients dying within five years.

"For patients with lung cancer, there are hardly any effective treatments available, so we investigated this unique compound that has activity against the AKT protein and found it to be extremely successful," said Krishna Menon, Ph.D., chief scientific officer of Cellceutix Corporation in Beverly, Mass.

Menon and colleagues tested the compound, which the company currently calls Kevetrin, in two human xenograft models: A549 and NCI-H1975, both of them multiple drug resistant. They tested 200 mg/kg of Kevetrin three times a day every other day against paclitaxel, one of the currently approved therapies for lung cancer, 22 mg/kg four times per day every other day.

In the A549 model, Kevetrin significantly delayed tumor growth by 11 days in the first experiment and by 30 days in a repeat experiment. By contrast, paclitaxel delayed growth by zero days in the first experiment and only three days in a subsequent experiment.

In the NCI-H1975 model, Kevetrin significantly delayed tumor growth by 34 days in the first experiment and by 28 days in a subsequent experiment. Similar to the previous model, paclitaxel delayed growth by just four and 14 days, respectively.

The researchers measured weight loss as a marker of toxicity and found it to be less than 5 percent in all experiments.

"It is encouraging that this drug has such little toxicity," said Menon.

#A25. Array-based comparative genomic hybridization of hepatocellular carcinoma reveals a unique genomic aberration pattern in tumors with poor prognosis

Scientists at the National Cancer Institute have identified a 10-gene signature that could predict survival in both liver and breast cancer, according to data presented at the American Association for Cancer Research Frontiers in Basic Cancer Research Meeting.

Stephanie Roessler, Ph.D., a visiting fellow in the Laboratory of Human Carcinogenesis at the NCI, and colleagues analyzed 13,000 genes to determine the genomic regions of human hepatocellular carcinoma (HCC) that are associated with poor prognosis. By integration of genomic aberration and gene expression they identified 10 potential tumor suppressor genes, which are associated with a 2.1-fold increased risk of death.

Tumor suppressor genes, as the name implies, prevent tumors when they are active.

"We and others found that genomic profiling of both liver cancer and breast cancer show overlapping regions of gain or loss," said Roessler. "When we analyze downstream pathways of these genes, we may be able to identify areas for more personalized medicine approaches in the future."

Roessler and colleagues performed their analysis in human liver and breast cancer tissue. Starting with 13,000 genes, they narrowed their search to 419 and then to 134 before determining the 10 that were significantly associated with impaired survival.

"We looked not only at the DNA copy number, but also at the gene expression, so this will help us identify genes that have a downstream function that can be manipulated by biologic therapies," said Roessler.

#A63. Inhibition of ROCK signaling inhibits breast cancer metastasis to human bone

Scientists have found that a kinase called ROCK is overexpressed in metastatic breast cancer, according to data presented at the AACR Frontiers in Basic Cancer Research Meeting. In this in vivo study, inhibiting ROCK in the earliest stages of breast cancer decreased metastasis by approximately 85 percent.

"This is preliminary research that will require further laboratory and clinical studies, but our results suggest that ROCK inhibition may be a drug therapy target for metastatic breast cancer," said Sijin Liu, Ph.D., a research instructor at Tufts University School of Medicine and the Sackler School of Graduate Biomedical Sciences at Tufts in Boston. Liu and colleagues used an experimental inhibitor called Y27632 to block ROCK action, which resulted in metastasis to the bone decreasing by approximately 85 percent.

The researchers used a mouse model with luminescent imaging to study the effects and found that Y27632 inhibited the overall frequency of metastasis by 36 percent compared to controls. Specifically, only five out of 14 tumors metastasized in treated mice compared with eight out of 12 in the control group.

The laboratory experiments suggested that ROCK inhibition may work by targeting a set of microRNAs. Those microRNAs, 17 through 92, were elevated in metastatic cells compared with non-metastatic cells and responded to treatment with Y27632.

"In this study, we showed that there is a specific microRNA cluster associated with ROCK expression and breast cancer metastasis," said Liu, who worked under the supervision of Michael Rosenblatt, M.D., professor of medicine and dean of Tufts University School of Medicine.

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The mission of the American Association for Cancer Research is to prevent and cure cancer. Founded in 1907, the AACR is the world's oldest and largest professional organization dedicated to advancing cancer research. The membership includes 30,000 basic, translational and clinical researchers; health care professionals; and cancer survivors and advocates in the United States and nearly 90 other countries. The AACR marshals the full spectrum of expertise from the cancer community to accelerate progress in the prevention, diagnosis and treatment of cancer through high-quality scientific and educational programs. It funds innovative, meritorious research grants, research fellowship and career development awards. The AACR Annual Meeting attracts more than 16,000 participants who share the latest discoveries and developments in the field. Special conferences throughout the year present novel data across a wide variety of topics in cancer research, treatment and patient care. The AACR publishes six major peer-reviewed journals: Cancer Research; Clinical Cancer Research; Molecular Cancer Therapeutics; Molecular Cancer Research; Cancer Epidemiology, Biomarkers & Prevention; and Cancer Prevention Research. The AACR also publishes CR, a magazine for cancer survivors and their families, patient advocates, physicians and scientists. CR provides a forum for sharing essential, evidence-based information and perspectives on progress in cancer research, survivorship and advocacy.

Media Contact:
Jeremy Moore
(267) 646-0557
In Boston, October 8-11:
(617) 457-2444